Neovascular glaucoma is a severe form of secondary glaucoma characterized by fibrovascular proliferation in the anterior chamber angle caused by chronic retinal ischemia. The most common causes are diabetic retinopathy, central retinal vein occlusion, and ocular ischemic disease. The proliferation of new blood vessels leads to the formation of a membrane that can cause open or closed angle glaucoma with very high intraocular pressure. Treatment involves controlling the underlying cause, lowering intraocular pressure through medications, laser treatment or surgery like trabeculectomy with anti-metabolites or tube shunts, and preventing further neovascularization through panretinal photocoagulation. Early diagnosis and aggressive treatment is important but successful management is challenging and

1. NEOVASCULAR GLAUCOMA
DR SIVATEJA CHALLA

2.  Definition
 History
 Etiology
 Pathophysiology
 Clinical course
 Clinical features
 DD’S
 Investigations
 Treatment

3. DEFINITION
Severe form of secondary glaucoma characterised by fibro vascular
proliferation in the anterior chamber angle.
SYNONYMS
1. Hemorrhagic glaucoma
2. Thrombotic glaucoma
3. Rubeotic glaucoma
4. Congestive glaucoma

4. HISTORY
1906  Coats , NVI in CRVO termed as RUBEOSIS IRIDIS
1937  Kurtz , NVA leading to PAS formation
1963  Weiss et al, coined the term NEOVASCULAR GLAUCOMA

5. ETIOLOGY
Diabetic retinopathy (M.C.C)
CRVO
Ocular ischemic disease

7. PATHOPHYSIOLOGY
CHRONIC RETINAL ISCHAEMIA
ANGIOGENIC FACTORS RELEASED &
DIFFUSED
NEOVASCULARISATION OF IRIS AND
ANGLE
NEOVASCULAR GLAUCOMA

8.  lens and vitreous acts as mechanical barriers and also releases vaso inhibitory
factors
So any complicated cat sx  PCR,APHAKIA more predisposition
VEGF  synthesised by all tissues in retina, mainly MULLERS CELL.
 VEGF conc 50-100 times more in aqueous humour in NVG

9. STAGES
 PRE RUBEOSIS
 PRE GLAUCOMA (RUBEOSIS IRIDIS )
 OPEN ANGLE GLAUCOMA
 ANGLE CLOSURE GLAUCOMA

10. Pre rubeosis stage
1. In patients with predisposing risk factors such as DR, CRVO, etc it is important
to understand the risk of developing rubeosis irides and the chances for
progression to NVG.
2. Look carefully for NVI and NVA under high ,magnification

11. Pre glaucoma stage : rubeosis iridis
a. NVI +/- NVA
b. IOP normal
c. Patients are asymptomatic
d. dilated tufts of preexisting
capillaries and fine, randomly
oriented vessels on the surface of
the iris near the pupillary margin

12. Open angle glaucoma
1. Elevated IOP
2. NVA and NVI increased
3. AC inflammatory reaction
4. Hyphema may be present
5. No PAS
6. Angles open
Fibro vascular fibrovascular membrane that
covers the angle and anterior surface of the iris
and may even extend onto the posterior iris
HALLMARK

13. Angle closure glaucoma
Most patients are detected in this stage
PAS formation
Fibro vascular membrane contarcts leads to
flat iris
Ectropion uveae present
IOP very high >60 mm hg

14. CLINICAL FEATURES
SYMPTOMS
- Severe pain
- Headache ,vomiting
- Redness
- Watering
- Defective vision
- Photophobia
SIGNS
- Reduced vision
- Ciliary injection
- Corneal oedema
- Deep AC with flare
- Hyphema
- Fixed dilated pupil
- NVI, NVA
- Raised IOP

16. Features Normal vessels New vessels
Location Iris stroma Pupillary margins
Angles
Arrangement Regular Irregualr
Appearance Tortuous Thin
Course Radial Arbourising
Character Not fenestrated Fenestrated
Scleral spur Not cross Crosses
Flouroscein No leakage leakage

17. DIFFERENTIAL DIAGONOSIS
1. PACG  no NVI and NVA
2. UVEITIC GLAUCOMA  KP’S + ,Complicated cataract, band shaped
keratopathy
3. FHI  stellate KP’S, NVA+ ,NVI and NVG are rare
4. ICE syndrome  corneal decompensation,correctopia,iris atrophy
5. Old trauma  angle recession,iris pigment clumps, no NVI
6. Lens induced glaucoma

18. INVESTIGATIONS
OCULAR :
- Fundus Fluorescein Angiogram- to assess retinal ischaemia
-Electroretinogram – to assess for retinal ischemia
-Iris angiography- in cases of doubtful NVI, to confirm the diagnosis
-B scan ultrasound- if view of retina not
SYSTEMIC :
- BP, FBS PPBS, Carotid Doppler, lipid profile,renal profile

19. TREATMENT
A. Identifying the underlying etiology and its timely and adequate treatment to
prevent the development and progression of NVG.
B. Once NVG develops and IOP is high, the major aspect of management is
control of high IOP to prevent optic nerve damage and continuous treatment
of underlying etiology.

20. Prophylactic treatment
Pan retinal photocoagulation (PRP)
DM  In established cases of PDR, PRP +/- IVB done to prevent NVG
And even after PRP, close f/u is needed
CRVO  PRP indicated only after 2 clock hours of NVA/NVI (CVOS)
OIS  PRP indicated for cases with retinal ischemia on FFA
 refer for neurological and cardiology assessment
Pan retinal photocoagulation
Make ischemic retina anoxic
Decreased angiognic factor
Decreased new vessels
Reduces AS neo vascularisation

21. Goniophotocoagulation
a. Adjunct to PRP
b. LASER therapy aimed at directly treating the NVA before development of NVG
c. No role once glaucoma is established
d. Low-energy argon laser treatments (0.2 seconds, 50-100 um, 100 - 200 mW)
are applied to the neovascular tufts as they cross the scleral spur.

22. Management of glaucoma
Medical management
Aqueous suppressants- beta blockers, carbonic anhydrase inhibitors, alpha agonists
Topical prostaglandin analogues can be tried though they may increase ocular inflammation
Miotics are contraindicated as they can increase inflammation and discomfort.
Frequent administration of are recommended to reduce inflammation that is inevitably
present topical steroids and cycloplegics .
Anti angiogenic drugs like bevacizumab intravitreal or intra cameral, reduces angiogenesis
and reduces inflammation

23. Management of glaucoma
Surgical management :
1. Medical management with intra vitreal anti-VEGF along with retinal ablation
wherever possible may be sufficient to control the IOP in the open angle
stage of NVG
2. But in advanced stage with synechial angle closure surgical intervention for
IOP lowering is often required.

24. Surgical management
 Trabeculectomy
 Tube shunts
 Cycloablation

25. Trabeculectomy :
a. Intraoperative use of anti-fibrotic agents is recommended to reduce the risk
of bleb failure due to subconjunctival scarring
b. The success rate of trabeculectomy with MMC in NVG at 1 year has been
reported to be around 62.6% and reduced to 51.7% at 5 years *
c. With the use of preoperative Bevacizumab, success rate may improve up to
95%**
* Takihara Y, Inatani M, Fukushima M, Iwao K, Iwao M, Tanihara H. Trabeculectomy with mitomycin C for
neovascular glaucoma: prognostic factors for surgical failure.Am J Ophthalmol 2009; 147:912–8.
** Saito Y, Higashide T, Takeda H, Ohkubo S, Sugiyama K.Beneficial effects of preoperative intravitreal
bevacizumab on trabeculectomy outcomes in neovascular glaucoma. Acta Ophthalmol 2010; 88:96–102.

26. Tube shunts
I. Glaucoma drainage devices are increasingly being considered as a primary
surgical procedure especially NVG where there is a high risk for failure of
conventional filtering surgery
II. Scarred conjunctiva, active inflammation, vigorous new vessel growth and
prior failure of trabeculectomy are also all indications to consider tube shunt
surgery in NVG.

27. Cycloablation :
For refractive NVG, no PL eye to relieve pain,
◦ Cyclocryotherapy.
◦ TSCPC, other contact and non contact trans scleral cyclo destructive procedures.
◦ Endoscopic cyclo photocoagulation.
12-24 burn spots ,posterior to limbus over
360 degrees , 1500-2000 MW, 1.5-2 secs.

29. Treatment
NVG
Seeing eye
NLP
- Medical Rx -
Cyclodestructive
procedure
Clear media
PRP
Poor media
Cryoablation
Vitreous hge
Vitrectomy+
endolaser
Trabeculectomy & Mitomycin
Tube shunts
cyclophotocoagulation

30. Conclusions
a. NVG is a potentially blinding disease
b. Early diagnosis and aggressive control of high IOP and the underlying etiology is crucial to
minimize the visual loss
c. Once IOP becomes elevated, successful management of disease becomes extremely difficult
d. No current medical or surgical treatment has a high success rate.

31. THANK YOU